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This review examines the molecular mechanisms underlying ASM-associated oxidative stress in clinical, non-kindled/kindled preclinical, as well as non-epilepsy models, and highlights evidence demonstrating the ability of ascorbic acid to attenuate ROS accumulation, enhance endogenous antioxidant defenses, and modulate redox-sensitive signaling pathways implicated in epileptogenesis and ASM-induced toxicity

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Compared with the recent probes with the similar backbone, the modification of the hydroxyl position herein resulted in the enhancement of the signal intensity at 485 nm with the excitation of 310 nm